leukotriene e-4

Leukotriene E-4 sulfone is a synthetic leukotriene.

Leukotriene E4 (LTE4) (LTE4) is produced by the action of dipeptidyl peptidase on LTD4 and is a component of the Slow Reactive Substance of Anaphylaxis (SRS-A).LTE4 is present in plasma and urine and can be used to detect asthma.

Leukotrienes (LTs) are a group of acute inflammatory mediators derived from arachidonic acid in leukocytes. The majority of these metabolites are formed through the 5-lipoxygenase (5-LO) pathway. 14,15-LTE4 is a metabolite of 14,15-LTC4 and 14,15-LTD4, an alternate class of LTs synthesized by a pathway involving the dual actions of 15- and 12-LOs on arachidonic acid via 15-HpETE and 14,15-LTA4 intermediates. These metabolites are classified as eoxins because they are formed mostly by eosinophils. Mast cells and nasal polyps can synthesize 14,15-LTC4 as well, however metabolism to 14,15-LTE4 in these cells and tissue has not been documented. 14,15-LTE4 increases vascular permeability of human endothelial cell monolayers with about 10-fold less potency than LTC4, but approximately 100-fold greater potency than histamine.

Maresin conjugates in tissue regeneration 1 (MCTR1) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is then converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase. MCTR1 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR1 (50 ng/mouse, i.p.) prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR1 reduces the amount of eicosanoids in the exudate.

Maresin conjugates in tissue regeneration 2 (MCTR2) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase then to MCTR2 by γ-glutamyl transferase. MCTR2 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR2 prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR2 selectively reduced the amount of the eicosanoids PGD2 and PGF2α in the exudate.

Maresin conjugates in tissue regeneration 3 (MCTR3) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages. DHA is oxidized to maresin 1 , which is converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase, then to MCTR2 by γ-glutamyl transferase, and to MCTR3 by dipeptidase. MCTR3 accelerates tissue regeneration in planaria (1 and 100 nM) approximately as potently as MCTR2 and more potently than MCTR1. Pretreatment with MCTR3 prior to E. coli administration in mice reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR3 selectively reduces the amount of the eicosanoids PGD2 , PGE2 , PGF2α , and TXB2 in the exudate.

N-acetyl Leukotriene E4 is an endogenous metabolite of Leukotriene E4, which is excreted mainly through bile, and is one to three orders of magnitude less active than Leukotriene E4, causing constriction of the airways.

Ritolukast (Wy-48252), an orally active aerosol leukotriene (LTD 4 E 4) receptor antagonist, effectively inhibits bronchoconstriction induced by aerosol LTD 4 in guinea pigs, demonstrating an ID 50 of 0.5mg kg [1].